Background The association between oral dysbiosis and chronic kidney disease (CKD) has gained increasing attention in recent years. Diabetes and hypertension are the most common conditions in CKD. However, a case–control study with matched confounding variables on the salivary microbiome in CKD and the influence of diabetes and hypertension on the microbiome has never been reported. Methods In our study, we compared the salivary microbiome profile between patients with CKD and healthy controls (HC) using 16S ribosomal DNA sequencing and examine its association with diabetes, hypertension, and immunity. Results We observed that the bacterial community was skewed in the saliva of CKD, with increased Lautropia and Pseudomonas, and decreased Actinomyces, Prevotella, Prevotella 7, and Trichococcus. No difference in the bacterial community between the CKD patients complicated with and without diabetes, and between those with and without hypertension. Prevotella 7 declined in CKD patients with/without hypertension with respect to HC, while Pseudomonas increased in CKD patients with/without hypertension. Pseudomonas was negatively associated with immunoglobin G in CKD patients. Both CKD patients with positive and negative antistreptolysin O had declined Prevotella 7 and Trichococcus compared to HC, whereas increased Pseudomonas. Conclusions Our study identifies a distinct bacterial saliva microbiome in CKD patients characterized by alteration in composition. We unravel here that the co-occurrence diseases of diabetes and hypertension are not associated with specific bacterial alterations, suggesting that bacterial dysbiosis in saliva plays a role in renal damage regardless of the occurrence of diabetes and hypertension.

Background High throughput 16S rRNA gene sequencing and enhanced culture methods (e.g., expanded quantitative urine culture, EQUC) have established the existence of the human bladder microbiome. We aim to test the hypothesis that the bladder environment of patients with chronic kidney disease (CKD) differs from that of unaffected controls with associated consequences for the composition of the bladder microbiome. Methods and Materials Females (n=66) and males (n=66) diagnosed with CKD and age-BMI-matched healthy control (HC) females (n=22) and males (n=22) were recruited. Transurethral catheterized urine was collected for 16S rRNA gene sequencing and Expanded Quantitative Urine Culture (EQUC). Fecal samples also were sequenced. Urinary analysis, kidney function and serum cytokines were examined. Results Bladder microbiomes of CKD females and males versus HC females and males differed (FDR<0.05); however, the difference was more obvious in females. In CKD females, sequencing revealed depletion of 5 genera, including Lactobacillus, and enrichment of 14 genera, including Escherichia/Shigella, Bifidobacterium, and several clostridial genera (FDR<0.05), while EQUC detected increased Escherichia and decreased Lactobacillus CKDB(P<0.05). Escherichia-Shigella was positively, whereas Lactobacillus was negatively, associated with CKDB-female serum creatinine (r=0.285, P=0.020; r=-0.337, P=0.006, respectively). Lactobacillus was positively associated with eGFR (r=0.251, P=0.042). Some CKD-related serum cytokines were negatively associated with clostridial genera. In contrast, the fecal microbiomes of CKD and HC females and males did not significantly differ in bacterial diversity or composition. However, bladder and fecal microbiomes of CKD females resembled each other more than those of controls, as assessed by the Bray-Curtis Dissimilarity Index (FDR<0.05). Conclusions CKD bladder microbiomes were dysbiotic, which was more obvious in females. This dysbiosis was associated with kidney damage severity and dysregulation of serum cytokines. The increased similarity between bladder and fecal microbiomes of CKD females suggests possible gut-leakage.

Backgrounds Microbial dysbiosis in the gut and urine has been implicated in patients with benign prostatic hyperplasia (BPH) based on previous studies. Additionally, emerging evidence has shown that salivary dysbiosis is associated with various diseases and oral health conditions. Building upon these findings, we aimed to investigate whether BPH patients exhibit a distinct salivary microbiome. Methods and Materials We recruited a cohort of BPH patients (n=50) and age-BMI matched healthy controls (HC; n=50). Salivary samples were collected for 16S rRNA gene sequencing, and prostate-specific antigen (PSA) levels were examined. Results Comparison of the salivary microbial communities between BPH patients and HC revealed significant differences, characterized by increased bacterial richness and diversity (FDR<0.05) in the BPH group. Further analysis identified the enrichment of 13 bacterial genera, including Clostridia-UCG-014, Oribacterium, and Filifactor, in BPH patients. Conversely, BPH patients exhibited a depletion of 4 bacterial genera, such as Actinomyces, Lachnoanaerobaculum, and Rothia(FDR<0.05). Several bacterial genera demonstrated potential as biomarkers for identifying BPH. Notably, we observed a negative correlation between the abundance of Oribacterium in BPH patients and the ratio of free PSA to total PSA (FPSA/TPSA) (r=-0.337, P=0.029). Conclusions Our findings indicate that the salivary microbiomes of BPH patients are dysbiotic. Moreover, we observed a significant association between this dysbiosis and dysregulation of PSA levels in BPH patients, suggesting the existence of a possible saliva-prostate axis. Modulating the salivary microbiome could potentially serve as an intervention strategy for BPH patients.

BackgroundTo establish antibiotic preregimes and administration routes for studies on urinary microbiota.Methods and materialsAntibiotics for enteritis (Abx-enteritis) and UTIs (Abx-UTI) were administered via gavage and/or urinary catheterisation (UC) for 1 and/or 2 weeks. The effects of these Abx on the urinary microbiota of rats were examined via 16S rRNA sequencing and urine culture, including anaerobic and aerobic culture. Additionally, the safety of the Abx was examined.ResultsAbx-enteritis/Abx-UTI (0.5 g/L and 1 g/L) administered via gavage did not alter the microbial community and bacterial diversity in the urine of rats (FDR &gt; 0.05); however, Abx-UTI (1 g/L) administered via UC for 1 and 2 weeks altered the urinary microbial community (FDR &lt; 0.05). Rats administered Abx-UTI (1 g/L) via UC for 1 week demonstrated a distinct urinary microbiota in culture. Abx-enteritis/Abx-UTI administered via gavage disrupted the microbial community and reduced bacterial diversity in the faeces of rats (FDR &lt; 0.05), and Abx-UTI administered via UC for 2 weeks (FDR &lt; 0.05) altered the fecal microbiota. Abx-UTI (1 g/L) administered via UC did not alter safety considerations. In addition, we noticed that UC did not induce infections and injuries to the bladder and kidney tissues.ConclusionsAdministration of Abx-UTI via UC for 1 week can be considered a pre-treatment option while investigating the urinary microbiota.